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Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE176417 | GEO | 2022/05/04

REPOSITORIES: GEO

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Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (RNA-Seq)

Project description:Unbiased whole-genome methylome was studied in the wound-edge (WE) tissue of chronic wound patients. Methylation status of proximal promoter (1Kb) was calculated using MethylCap-Seq and PrEMeR-CG data analyses. A total of 4689 differentially methylated regions (DMRs) were identified in chronic WE compared to unwounded (UW) human skin. Hypermethylation was more frequently observed (3661 DMRs) in the chronic WE compared to hypomethylation (1028 DMRs). Twenty-six hypermethylated DMRs were involved in epithelial to mesenchymal transition (EMT). Bisulfite sequencing validated hypermethylation of a predicted specific upstream regulator TP53. Whole genome RNA sequencing analysis was performed to qualify findings from methylome analysis. Hierarchical clustering analyses identified a large set of genes, the expression of which were significantly downregulated in chronic WE compared to UW skin. Analysis of the downregulated genes identified the TP53 signaling pathway, including P63, P73, FOXO3, SIRT1 and HDAC1, as being significantly silenced. Direct comparison of hypermethylation and downregulated gene expression identified four genes, ADAM17, NOTCH, TWIST1 and SMURF1, that were common to both data sets and functionally represented the EMT pathway. Single cell RNA sequencing studies identified that these effects on gene expression were limited to the keratinocyte cell compartment.

2022-05-04 | GSE176414 | GEO

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (MethylCap-seq)

2022-05-04 | GSE176413 | GEO

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (Spatial RNA-Seq)

2022-05-04 | GSE176416 | GEO

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (single cell RNA-Seq)

2022-05-04 | GSE176415 | GEO

Genome-wide DNA hypermethylation opposes healing in patients with chronic wounds by impairing epithelial-mesenchymal transition.

Project description:An extreme chronic wound tissue microenvironment causes epigenetic gene silencing. An unbiased whole-genome methylome was studied in the wound-edge tissue of patients with chronic wounds. A total of 4,689 differentially methylated regions (DMRs) were identified in chronic wound-edge skin compared with unwounded human skin. Hypermethylation was more frequently observed (3,661 DMRs) in the chronic wound-edge tissue compared with hypomethylation (1,028 DMRs). Twenty-six hypermethylated DMRs were involved in epithelial-mesenchymal transition (EMT). Bisulfite sequencing validated hypermethylation of a predicted specific upstream regulator TP53. RNA-Seq analysis was performed to qualify findings from methylome analysis. Analysis of the downregulated genes identified the TP53 signaling pathway as being significantly silenced. Direct comparison of hypermethylation and downregulated genes identified 4 genes, ADAM17, NOTCH, TWIST1, and SMURF1, that functionally represent the EMT pathway. Single-cell RNA-Seq studies revealed that these effects on gene expression were limited to the keratinocyte cell compartment. Experimental murine studies established that tissue ischemia potently induces wound-edge gene methylation and that 5'-azacytidine, inhibitor of methylation, improved wound closure. To specifically address the significance of TP53 methylation, keratinocyte-specific editing of TP53 methylation at the wound edge was achieved by a tissue nanotransfection-based CRISPR/dCas9 approach. This work identified that reversal of methylation-dependent keratinocyte gene silencing represents a productive therapeutic strategy to improve wound closure.

| S-EPMC9433101 | biostudies-literature

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition

Project description:Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition

| PRJNA736091 | ENA

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (MethylCap-seq)

Project description:Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (MethylCap-seq)

| PRJNA736093 | ENA

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (RNA-Seq)

Project description:Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (RNA-Seq)

| PRJNA736094 | ENA

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (Spatial RNA-Seq)

Project description:Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (Spatial RNA-Seq)

| PRJNA736096 | ENA

Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (single cell RNA-Seq)

Project description:Genome-Wide DNA Hypermethylation in the Wound-Edge of Chronic Wound Patients Opposes Closure by Impairing Epithelial to Mesenchymal Transition (single cell RNA-Seq)

| PRJNA736095 | ENA

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